Monitoring disease activity by stool analyses: from occult blood to molecular markers of intestinal inflammation and damage

Foell, Dirk; Wittkowski, Helmut; Roth, Johannes

doi:10.1136/gut.2008.170019

Cited by 193 publications

(176 citation statements)

References 100 publications

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“…It activates Toll-like receptor 4 (TLR4) and thereby amplifies inflammatory activity (11). In gastroenterology, fecal calprotectin concentration is used to differentiate between inflammatory bowel diseases (high calprotectin concentration) and merely functional disorders, such as irritable bowel syndrome (low calprotectin concentration) (12,13). Our findings show that prerenal AKI constitutes the renal analogue to irritable bowel syndrome.…”

Section: Discussionmentioning

confidence: 97%

Urinary Calprotectin and the Distinction between Prerenal and Intrinsic Acute Kidney Injury

Heller¹,

Frischmann²,

Grünbaum³

et al. 2011

Clinical Journal of the American Society of Nephrology

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SummaryBackground and objectives To date there is no reliable marker for the differentiation of prerenal and intrinsic acute kidney injury (AKI). We investigated whether urinary calprotectin, a mediator protein of the innate immune system, may serve as a diagnostic marker in AKI.Design, setting, participants, & measurements This was a cross-sectional study with 101 subjects including 86 patients with AKI (34 prerenal, 52 intrinsic including 23 patients with urinary tract infection) and 15 healthy controls. Assessment of urinary calprotectin concentration was by ELISA and immunohistochemistry of kidney biopsy specimens using a calprotectin antibody. Inclusion criteria were: admission to hospital for AKI stage 1 to 3 (Acute Kidney Injury Network); exclusion criteria were: prior renal transplantation and obstructive uropathy.Results Median urinary calprotectin was 60.7 times higher in intrinsic AKI (1692 ng/ml) than in prerenal AKI (28 ng/ml, p Ͻ0.01). Urinary calprotectin in prerenal disease was not significantly different from healthy controls (45 ng/ml, p ϭ 0.25). Receiver operating curve curve analysis revealed a high accuracy of calprotectin (area under the curve, 0.97) in predicting intrinsic AKI. A cutoff level of 300 ng/ml provided a sensitivity of 92.3% and a specificity of 97.1%. Calculating urinary calprotectin/creatinine ratios did not lead to a further increase of accuracy. Immunostainings of kidney biopsies were positive for calprotectin in intrinsic AKI and negative in prerenal AKI.Conclusions Accuracy of urinary calprotectin in the differential diagnosis of AKI is high. Whereas calprotectin levels in prerenal disease are comparable with healthy controls, intrinsic AKI leads to highly increased calprotectin concentrations.

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Section: Discussionmentioning

confidence: 97%

Urinary Calprotectin and the Distinction between Prerenal and Intrinsic Acute Kidney Injury

Heller¹,

Frischmann²,

Grünbaum³

et al. 2011

Clinical Journal of the American Society of Nephrology

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“…It is a very sensitive and specific marker of localized inflammatory processes, such as gastrointestinal inflammation,128 and can be increased in serum with various inflammatory disorders 47, 116, 118, 129, 130. In contrast to calprotectin, corticosteroid treatment does not affect serum S100A12 concentrations 131…”

Section: Biomarkers In Chronic Inflammatory Enteropathies Of Dogsmentioning

confidence: 99%

Clinical utility of currently available biomarkers in inflammatory enteropathies of dogs

Heilmann

Steiner

2018

Veterinary Internal Medicne

108

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Chronic inflammatory enteropathies (CIE) in dogs are a group of disorders that are characterized by chronic persistent or recurrent signs of gastrointestinal disease and histologic evidence of mucosal inflammation. These CIEs are classified as either food‐responsive, antibiotic‐responsive, or immunosuppressant‐responsive enteropathy. Patients not clinically responding to immunomodulatory treatment are grouped as nonresponsive enteropathy and dogs with intestinal protein loss as protein‐losing enteropathy. Disease‐independent clinical scoring systems were established in dogs for assessment of clinical disease severity and patient monitoring during treatment. Histopathologic and routine clinicopathologic findings are usually not able to distinguish the subgroups of CIE. Treatment trials are often lengthy and further diagnostic tests are usually at least minimally invasive. Biomarkers that can aid in defining the presence of disease, site of origin, severity of the disease process, response to treatment, or a combination of these would be clinically useful in dogs with CIE. This article summarizes the following biomarkers that have been evaluated in dogs with CIE during the last decade, and critically evaluates their potential clinical utility in dogs with CIE: functional biomarkers (cobalamin, methylmalonic acid, folate, α1‐proteinase inhibitor, immunoglobulin A), biochemical biomarkers (C‐reactive protein, perinuclear anti‐neutrophilic cytoplasmic antibodies, 3‐bromotyrosine, N‐methylhistamine, calprotectin, S100A12, soluble receptor of advanced glycation end products, cytokines and chemokines, alkaline phosphatase), microbiomic biomarkers (microbiome changes, dysbiosis index), metabolomic biomarkers (serum metabolome), genetic biomarkers (genomic markers, gene expression changes), and cellular biomarkers (regulatory T cells). In addition, important performance criteria of diagnostic tests are briefly reviewed.

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“…Disease relapses decrease the quality of life of affected individuals. In the last few decades, studies have focused on the identification of possible factors, including the neutrophil Fcγ receptor I (CD64) index, anti-GM-CSF antibody (Ab) levels, serum levels of ficolin-2, fecal calprotectin and Clostridium difficile presence, that may correlate with disease activity and predict disease relapse (5)(6)(7)(8)(9)(10). However, to the best of our knowledge, none of the previously investigated factors were found to be reliable indicators of disease activity.…”

Section: Introductionmentioning

confidence: 99%

Gene expression alterations in inflamed and unaffected colon mucosa from patients with mild inflammatory bowel disease

Lian

et al. 2016

Molecular Medicine Reports

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Abstract. An endoscopic examination is currently the most reliable method for monitoring disease activity in patients with inflammatory bowel disease (IBD). However, endoscopic evaluations are unable to detect mucosal inflammation at the earliest stages. The present study aimed to evaluate the molecular profiles of inflamed and unaffected colon mucosa from patients with mild Crohn's disease (CD) and ulcerative colitis (UC), in order to identify a more sensitive method for monitoring mucosal impairment. Patients were recruited and colon biopsies from the inflamed and the normal-appearing mucosa of patients with mild IBD were obtained by colonoscopy. Gene expression analysis was performed using microarrays, after which Gene Ontology and clustering were performed using bioinformatics. In addition, the levels of inflammatory cytokines were analyzed by reverse transcription-quantitative polymerase chain reaction. A total of 620 genes in the inflamed and 210 genes in the unaffected colon mucosa with at least a 3-fold change, as compared with healthy controls, were detected in patients with mild CD, and 339 genes in the inflamed and 483 genes in the unaffected colon mucosa were detected in patients with mild UC. Heat mapping demonstrated a similarity in the gene alteration patterns, and altered transcripts overlapped, between the inflamed and unaffected colon mucosa. Interferon-γ and interleukin-17 mRNA levels were comparably elevated in the inflamed and unaffected colon mucosa from patients with IBD. Marked gene expression alterations were detected in the inflamed and unaffected colon mucosa from patients with mild IBD, and these showed marked similarity and overlap between the two groups. The results of the present study suggested that inflammation was not limited to the endoscopic lesions and that gene expression profiling may be considered a sensitive tool for monitoring mucosal inflammation, predicting relapses and optimizing therapeutic strategies for patients with IBD.

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Monitoring disease activity by stool analyses: from occult blood to molecular markers of intestinal inflammation and damage

Cited by 193 publications

References 100 publications

Urinary Calprotectin and the Distinction between Prerenal and Intrinsic Acute Kidney Injury

Urinary Calprotectin and the Distinction between Prerenal and Intrinsic Acute Kidney Injury

Clinical utility of currently available biomarkers in inflammatory enteropathies of dogs

Gene expression alterations in inflamed and unaffected colon mucosa from patients with mild inflammatory bowel disease

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